There are many similarities between the biochemistry of the erythrocyte and the lens of the eye because both are non-nucleated cells. Homozygous deficiency of either galactokinase of galactose-1-phosphate uridyl transferase produce cataracts early in life and can be detected by enzymatc measurements in red blood cells. We postulated that the heterozygous deficiency of these enzymes and perhaps other related abnormalities might be responsible for the development of presenile cararacts and that appropriate medical treatment might halt the development of the cataract. A pilot study of patients with presenile cataracts has shown a high prevalence of heterozygotes for the inborn errors of galactose metabolism and patients with evidence of riboflavin deficiency in erythrodytes. We plan to identify heterozygotes in a large population of patients with presenile cataracts to quanitify the incidence of these abnormalities and to ascertain if a low galactose diet will show the progression of their cataracts. Similarly, riboflavin will be administered to half the population with evidence of diminshed erythrocyte riboflavin and followup will be undertaken to determine if this diminishes the rate of cataract growth. A population of black diabetics will be studied to quantify the prevalence of cataracts and determine if G-6-PD deficiency influences the occurrence of cataracts. A colony of rodents which readily develop cataracts (Octodon Degus) has been established and will be used to study the interaction of riboflavin deficiency, diabetes and galactosemia in this animal model.